Abstract

It has been shown that circular RNA XPO1 (circXPO1) is involved in cancer (e.g., lung adenocarcinoma and osteosarcoma) progression by sponging microRNAs. Nevertheless, the role of circXPO1 and its interaction with microRNAs in prostate cancer remains unknown. In this study, the results of quantitative real-time PCR showed that circXPO1 levels were dramatically increased in human prostate cancer tissue and cell lines compared with those in normal tissue and cell line. Furthermore, cell proliferation, colony formation, and cell invasion assays showed that circXPO1 promoted the malignant behavior of pancreatic cells in vitro. Mechanistically, bioinformatics prediction, a dual-luciferase reporter assay, and pull-down assay suggested that circXPO1 physically targets miR-23a and negatively regulates its expression in pancreatic cancer cells. miR-23a mimics and inhibitors effectively reversed the effects of circXPO1 on the malignant behavior of prostate cancer cells in vitro. Consistent results were observed in the xenograft tumor model. In conclusion, circXPO1 promotes prostate cancer progression via targeting miR-23a, thus suggesting the circXPO1/miR-23a axis can be used as a potential therapeutic target for prostate cancer treatment.

Highlights

  • Prostate cancer is the second most common cancer and the fifth leading cause of cancer-related death in men worldwide [1]

  • To investigate the expression of circXPO1 in prostate carcinoma, we examined the expression of circXPO1 in prostate cancer tissue and cell lines

  • This study demonstrated that circXPO1 levels were significantly increased in human prostate cancer tissue and prostate cancer cell lines compared with those in corresponding controls

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Summary

Introduction

Prostate cancer is the second most common cancer and the fifth leading cause of cancer-related death in men worldwide [1]. For patients with primary prostate cancer, prostatectomy is commonly used. Patients with early-stage diseases generally have good prognoses, up to 30% of cases suffer relapses within 5–10 years posttreatment. The 5-year relative survival is around 30% for patients with distant metastasis [2, 3]. Inflammation is an initial process in which cells are trafficked into the tumor microenvironment by specific cytokines called chemokines. This recruitment is complex and involves multiple subsets of white blood cells with anti-cancer and anti-cancer functions in the progress from benign prostatic enlargement to prostate cancer [4, 5]. Androgen deprivation therapy is the first-line therapy for recurrent or metastatic prostate cancer. It is of urgent importance to identify novel therapeutic strategies for the treatment of prostate cancer

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